Taken together, our data reveal that starvation-induced 14-3-3γ is required for β-catenin-Beclin-1-LC3-autophagy in starved neurons in vitro and in vivo, which may provide insights in the treatment of neurologic diseases such as stoke.
Additionally, miR-124 stimulated Wnt/β-catenin signaling via suppressing DACT1 expression. miR-124 promoted proliferation and induced NSC differentiation to neurons by activation of Wnt/β-catenin pathway via targeting DACT1, providing a potential target and aiding the development of cell-based therapies for neurological disorders.
A thorough understanding of interactions between β-catenin and its binding partners will enable us to more effectively understand how β-catenin switches between its multiple roles, and will lead to the development of specific assays for the identification of small molecules as chemotherapeutic agents to treat diseases, including cancer and neurological disorders, where Wnt/β-catenin signaling is dysregulated.